Individuals who suffer head trauma from sports, accidents, or other causes often go on to develop neurodegenerative diseases like Parkinson's or Alzheimer's. A new study sheds light on why that might be and offers a way to prevent it.
Suffering a head trauma like one delivered from a particularly fierce tackle in football, or a punch in boxing, can cause all kinds of pain and problems immediately after impact – including concussion or compressed spinal vertebrae. But such blows have also been linked to the development of longer-term issues, including dementia and other neurodegenerative diseases.
After conducting a study, researchers at Tuft's University and Oxford University now believe this is because blows to the head might awaken the normally dormant herpes simplex virus 1 (HSV-1) in the brain.
While most often associated with the blisters or ulcers it causes after being spread through oral contact and becoming an active infection, the fact is that over 80% of all people already have this bug inside of them. For many people the virus simply stays sleeping inside our neurons and brain cells, not causing any harm.
But HSV-1 has also been linked to the development of Alzheimer's disease. In previous studies the activation of the virus in brain tissue in the lab led to the hallmarks of the condition, including the development of amyloid plaques, the degradation of neurons, and the impairment of the overall neural network.
Because both head trauma and HSV-1 activation are linked to Alzheimer's, the Tuft's and Oxford researchers set out to see if there was a connection.
“We thought, what would happen if we subjected the brain tissue model to a physical disruption, something akin to a concussion?," said lead author Dana Cairns from Tuft's. "Would HSV-1 wake up and start the process of neurodegeneration?”
Brain sponge
To start, they built a sort of model brain in the lab consisting of a spongy material made from collagen and silk protein. After infusing this donut-shaped sponge with neural stem cells, the team allowed them to develop into an entire neural network, complete with neurons, axons, dendrites, and glial cells, which are brain cells that help support the neurons. All of these cells began communicating with each other as they would inside an actual brain and, just like an actual brain, some of the cells held dormant HSV-1 viral DNA within them .
The brain sponge was then placed inside a cylinder that was subjected to a blow by a piston to simulate a concussion.
Sure enough, after the impacts from the piston, the HSV-1 cells became active and began causing their usual havoc – sparking inflammation, fostering the growth of tangle-causing amyloid plaques, killing off neurons, and leading to a runaway development of glial cells in a process called gliosis.
After seeing this effect, the researchers posit that it is indeed likely that blows to our actual brains awaken the HSV-1 virus and lead to the development of Alzheimer's. As a result, they believe it might be possible to stem the advancement of the condition following head trauma through the administration of antiviral or anti-inflammatory drugs.
“The brain tissue model takes us to another level in investigating these connections between injury, infection, and Alzheimer’s disease,” said study co-author David Kaplan from Tuft's.
“We can recreate normal tissue environments that look like the inside of a brain, track viruses, plaques, proteins, genetic activity, inflammation and even measure the level of signaling between neurons,” he added. “There is a lot of epidemiological evidence about environmental and other links to the risk of Alzheimer’s. The tissue model will help us put that information on a mechanistic footing and provide a starting point for testing new drugs.”
The study has been published in the journal Science Signaling.
Source: Tuft's University
